ArticleNature medicine2013
Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models.
Article in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 119 citations in OpenAlex.
- Integrative MRI and Genomics Analyses PrioritizeAnimals : an open access journal from MDPI · 2026Article
- Huntingtin and its allies at the cortico-striatal synapse.Cell death & disease · 2026Review
- UCM-A86 is a selective positive allosteric modulator of GluN1/GluN3 NMDA receptors.Molecular pharmacology · 2026Article
- Discovery of selective GluN1/GluN3A NMDA receptor inhibitors using integrated AI and physics-based approaches.Acta pharmacologica Sinica · 2026Article
- New advances in small molecule drugs targeting NMDA receptors.Acta pharmacologica Sinica · 2026Review
- AI-enhanced virtual screening approach to hit identification for GluN1/GluN3A NMDA receptor.Acta pharmacologica Sinica · 2026Article
- The GluN3-containing NMDA receptors.Channels (Austin, Tex.) · 2025Review
- UCM-A86 is a selective positive allosteric modulator of GluN1/GluN3 NMDA receptors.bioRxiv : the preprint server for biology · 2025Article
- Contrastive learning-based drug screening model for GluN1/GluN3A inhibitors.Acta pharmacologica Sinica · 2025Article
- Discovery of novel GluN1/GluN3A NMDA receptor inhibitors using a deep learning-based method.Acta pharmacologica Sinica · 2025Article
- Discrete interneuron subsets participate in GluN1/GluN3A excitatory glycine receptor (eGlyR)-mediated regulation of hippocampal network activity throughout development and evolution.Research square · 2025Article
- Discrete interneuron subsets participate in GluN1/GluN3A excitatory glycine receptor (eGlyR)-mediated regulation of hippocampal network activity throughout development and evolution.bioRxiv : the preprint server for biology · 2025Article
- Alterations of NMDAR Subunits in the Cerebrospinal Fluid Across Neurodegenerative and Immunological Disorders.Journal of neurochemistry · 2025Article
- NMDA receptors in neurodegenerative diseases: mechanisms and emerging therapeutic strategies.Frontiers in aging neuroscience · 2025Review
- Synaptic and extrasynaptic distribution of NMDA receptors in the cortex of Alzheimer's disease patients.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- GluN3A and Excitatory Glycine Receptors in the Adult Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- A Neuroligin-1 mutation associated with Alzheimer's disease produces memory and age-dependent impairments in hippocampal plasticity.iScience · 2023Article
- Allosteric modulation of GluN1/GluN3 NMDA receptors by GluN1-selective competitive antagonists.The Journal of general physiology · 2023Article
- Activation of excitatory glycine NMDA receptors: At the mercy of a whimsical GluN1 subunit.The Journal of general physiology · 2023Article
- Early TNF-Dependent Regulation of Excitatory and Inhibitory Synapses on Striatal Direct Pathway Medium Spiny Neurons in the YAC128 Mouse Model of Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 10 institutions in 7 countries.
Funding
Abstract
Huntington's disease is caused by an expanded polyglutamine repeat in the huntingtin protein (HTT), but the pathophysiological sequence of events that trigger synaptic failure and neuronal loss are not fully understood. Alterations in N-methyl-D-aspartate (NMDA)-type glutamate receptors (NMDARs) have been implicated. Yet, it remains unclear how the HTT mutation affects NMDAR function, and direct evidence for a causative role is missing. Here we show that mutant HTT redirects an intracellular store of juvenile NMDARs containing GluN3A subunits to the surface of striatal neurons by sequestering and disrupting the subcellular localization of the endocytic adaptor PACSIN1, which is specific for GluN3A. Overexpressing GluN3A in wild-type mouse striatum mimicked the synapse loss observed in Huntington's disease mouse models, whereas genetic deletion of GluN3A prevented synapse degeneration, ameliorated motor and cognitive decline and reduced striatal atrophy and neuronal loss in the YAC128 Huntington's disease mouse model. Furthermore, GluN3A deletion corrected the abnormally enhanced NMDAR currents, which have been linked to cell death in Huntington's disease and other neurodegenerative conditions. Our findings reveal an early pathogenic role of GluN3A dysregulation in Huntington's disease and suggest that therapies targeting GluN3A or pathogenic HTT-PACSIN1 interactions might prevent or delay disease progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.